Covid can activate dormant bacterial infection, TB: Study
The study, led by researchers from the Indian Institute of Technology, Guwahati, and University of Massachusetts, showed that infection with a specific coronavirus strain reactivated dormant Mycobacterium tuberculosis (MTB) in mice.
Guwahati: The SARS-CoV-2 virus that causes Covid-19, may have the ability to reactivate dormant tuberculosis (TB), according to study that is an alarming news for countries like India, which accounts for an estimated 40 per cent of the population with dormant or latent TB.
The study, led by researchers from the Indian Institute of Technology, Guwahati, and University of Massachusetts, showed that infection with a specific coronavirus strain reactivated dormant Mycobacterium tuberculosis (MTB) in mice.
The results, detailed in the The American Journal of Pathology, may pave the way for new vaccines against the infectious disease and avoid a potential global TB epidemic.
“The finding of TB reactivation in a stem cell-mediated Mtb dormancy mouse model during MHV-1 coronavirus infection indicates that in the long-term, post-pandemic, the SARS-CoV-2 virus might activate dormant bacterial infections. This is a significant finding considering the current coronavirus pandemic, where many individuals in India and other developing countries with dormant TB infection may see an increase in active TB cases post Covid-19,” explained lead investigator Bikul Das, from Department of Stem Cell and Infectious Diseases, KaviKrishna Laboratory, IIT-Guwahati.
“There is an urgent need to study the association of Covid-19 with dormant TB reactivation to avoid a potential global TB pandemic,” Das added.
For the study, the team studied the coronavirus strain murine hepatitis virus-1 (MHV-1) infection in the lung in a mouse model (dMtb) of mesenchymal stem cell (MSC)-mediated MTB dormancy. This showed 20-fold lower viral loads than the dMtb-free control mice by the third week of viral infection and a six-fold increase of altruistic stem cells (ASCs), thereby enhancing the defense.
TB was reactivated in the dMtb mice, suggesting that dormant TB bacteria hijack these ASCs to replicate in the lung to cause pulmonary TB. Results suggest that these ASCs are transient (they expand for two weeks and then undergo apoptosis or cellular suicide) and exhibit antiviral activities against MHV-1 by secreting soluble factors.
“It is important to understand the host defence mechanism against this disease to develop a better vaccine and/or treatment. We therefore postulated that, similar to bacteria, adult stem cells may also exhibit an altruistic defence mechanism to protect their niche against external threat,” Das said.
